See figure 31-7 [WG21:p607]
... of neurons mediating sympathetic discharge to CVS
Located near the pial surface of the medulla in the rostral ventrolateral medulla (RVLM).
Axons travel dorsally and medially, then descend in the lateral column of the spinal cord
Project to the sympathetic preganglionic neurons in the intermediolateral gray column (IML) of the spinal cord
Preganglionic neurons then innervate
Postganglionic sympathetic neurons then innervate the heart and blood vessels
* Neurotransmitter: NE
A. Directly stimulated by
(Presumably directly on RVLM)
B. Excitatory inputs
C. Inhibitory inputs
D. Other factors
(via vagal afferent)
--> Vasodilation and decreased BP
--> Increase BP via reticular formation[WG21:p606]
But prolonged pain
--> Vasodilation and fainting
... refers to stimulation of somatic afferent nerve causing pressor response
Probably via C1 neurons in the RVLM
[WG21:p612]
Stimulation of peripheral chemoreceptor (e.g. in stagnant hypoxia due to hemorrhage) leads to
Stimulation of central chemoreceptor (e.g. by increased PaCO2, decrease pH)
--> Vasoconstriction
[BL8:p192]
NB:
Direct effect of hypoxia is small (compared with effects of hypercapnia)
Increase in PaCO2 stimulates vasomotor area
--> Vasoconstriction
But,
Increase in PaCO2 directly causes peripheral vasodilation
* Especially in skin and brain
Overall,
--> Slow rise in BP
When ICP is increased
--> Impaired blood perfusion
--> Hypoxia and hypercapnia in vasomotor area
--> Increase in BP (Cushing reflex)
--> Reflex decrease in HR (via baroreceptors)
Thus, increased ICP is characterised by bradycardia
Respiration also slowed [WG21:p621]
[WG21: p613]
Originates in cerebral cortex
--> Relays in hypothalamus and mesencephalon
--> Passes through (without synapsing) IML gray column of spinal cord
--> Synapse with postganglionic cholinergic neurons to blood vessels
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